SAN DIEGO -- The end of the nationwide fungal meningitis outbreak is not yet in sight as the number of cases continues to rise, a CDC official said here.

SAN DIEGO – The end of the nationwide fungal meningitis outbreak is not yet in sight, a CDC official said here, as the number of cases rose to 271 and the death toll hit 21.

"I think we're talking about being vigilant for months," according to Thomas Chiller, MD, deputy chief of the agency's mycotic diseases branch.

He said the period from injection of the tainted steroid -- preservative-free methylprednisolone acetate – to the onset of symptoms is thought to range from 4 to 42 days, based on known cases so far.

But in a similar outbreak in 2002, Chiller told a panel at IDWeek 2012, the longest incubation period was 152 days, "so I think we need to be cautious."

His warning came as the CDC reported an additional 14 cases, with one more death. Three of the cases involve peripheral joint infections, while the rest involve fungal meningitis.

Meanwhile, clinicians from Vanderbilt University School of Medicine in Nashville, Tenn., described their battle to save a man in his 50s who would become the index case the outbreak.

Online in the New England Journal of Medicine, they recounted the measures they took – ultimately in vain – to find a cause and a treatment for the meningitis that afflicted the man.

It was their discovery of an infection with the fungus Aspergillus fumigatus that led them to alert the Tennessee health department and to the recognition of the outbreak.

Mysteriously, the man is the only patient so far in which Aspergillus is thought to be the cause of disease.

The organism apparently involved in most cases so far is Exserohilum rostratum, which, according to Thomas Patterson, MD, of the University of Texas Health Science Center in San Antonio, only rarely causes human disease.

When it does, he told attendees at the IDWeek panel, the illness is usually superficial -- allergic sinusitis, for instance, or soft tissue infections. "But beyond question, there are a number of black molds that can cause neurologic disease," he said.

A case in point is the outbreak 10 years ago involving a different black mold, Exophiala dermatitidis.

That outbreak parallels current events in many ways, according to John Perfect, MD, of Duke University Medical Center.

In that year, the CDC reported five cases of Exophiala (Wangiella) dermatitidis meningitis or arthritis that were linked to contaminated preservative-free methylprednisolone acetate prepared by a compounding pharmacy, Perfect noted online in Annals of Internal Medicine.

"We learned, or thought we learned, several important lessons from the outbreak," Perfect wrote:

"However," Perfect argued, "the cost in patient worry and suffering, medical expenses, and public health surveillance of the 2002 outbreak was high, and the public's trust that medications are safe from microbial contamination was shaken."

The parallels are clear and – as in 2002 – those dealing with the current outbreak are working mainly in the dark.

"The details of the epidemiology, including the attack rate, remain unclear," Perfect wrote. "Individual physicians cannot wait for definitive answers and must act decisively at an early stage of infection."

In the index case, according to April Pettit, MD, and colleagues at Vanderbilt, the man complained of headache and neck pain that had become progressively worse over the course of eight days, as well as nausea, malaise, fatigue, chills, and decreased appetite.

Four weeks earlier, he had been given the last of a series of epidural injections of methylprednisolone acetate for low back pain, Pettit and colleagues reported.

The patient was admitted to the hospital and started on empiric antibiotics and glucocorticoids, but when the routine blood and CSF bacterial cultures were negative, the steroids were stopped, the clinicians reported.

The man's symptoms appeared to improve and he was sent home on vancomycin and ceftriaxone for presumed community-acquired meningitis. He returned a week later with worsened symptoms, including incomprehensible speech.

A repeat lumbar puncture showed that the CSF protein level was more than twice as high as before, the glucose concentration was one-fifteenth what it had been, and the white blood cell count had doubled.

Antibiotic therapy again initially improved the symptoms, Pettit and colleagues reported, but they worsened again, including, on the sixth day of admission, increased somnolence, intermittent staring spells, and a transient right facial droop. The clinicians added empiric amphotericin B to the antibiotics.

On the seventh day of his second hospital stay, the lab reported finding Aspergillus in the CSF and Pettit and colleagues added intravenous voriconazole to the amphotericin B.

In subsequent days, MRI and CT scans revealed infarcts in the midbrain and cerebellum, intraventricular and subarachnoid hemorrhaging, and worsening hydrocephalus.

"Despite improving findings on cerebrospinal fluid testing and control of seizure activity, there was no meaningful neurologic recovery," the clinicians reported, and on day 15 of admission, the man's family agreed to withdraw life support. He died a week later.